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Decabromodiphenyl ether induces male reproductive toxicity by activating mitochondrial apoptotic pathway through glycolipid metabolism dysbiosis
Zhang, Yue1,2; Li, Xiangyang1,2; Jing, Li1,2; Zhou, Guiqing1,2; Sang, Yujian1,2; Gao, Leqiang1,2; Jiang, Shuqin1,2; Shi, Zhixiong1,2; Ge, Wei3; Sun, Zhiwei1,2; Zhou, Xianqing1,2
2021-12-01
Source PublicationChemosphere
ISSN0045-6535
Volume285
Abstract

Decabromodiphenyl ether (BDE-209), an extensively used flame retardant, exists widely in the environment. Although male reproductive toxicity induced by BDE-209 has been reported, its mechanisms remain unclear. To explore the role of glycolipid metabolism in male reproductive toxicity and the potential mechanisms, forty male SD rats were divided into four groups and given gavage with BDE-209 at 0, 5, 50, and 500 mg/kg/d for 28 days. In vitro, the spermatogenic cell lines GC-2spd cells were divided into four groups: the control group, 32 μg/mL BDE-209 group, 32 μg/mL BDE-209 + 0.4 μM Fatostatin (the inhibitor of SREBP-1) group, and 0.4 μM Fatostatin group. Our results showed that BDE-209 decreased sperm quality and quantity, which was correlated with glycolipid metabolism dysbiosis of testis. The levels of glucose, triglyceride, and total cholesterol were negatively correlated with sperm concentration, and triglyceride and total cholesterol levels were negatively correlated with sperm motility, while positively correlated with the sperm malformation rate. Moreover, BDE-209 exposure activated the glycolipid metabolism pathways (PPARγ/RXRα/SCAP/SREBP-1) and mitochondrial apoptotic pathway, thereby inducing the apoptosis of spermatogenic cells. In vitro, BDE-209 caused triglyceride and total cholesterol disorder and apoptosis of GC-2spd cells, the lipid metabolism pathways inhibitor fatostain downregulated the elevation of triglyceride and total cholesterol concentrations, and suppressed apoptosis and the activation of the mitochondrial apoptotic pathway in GC-2spd cells caused by BDE-209. Our results indicated that BDE-209 induced male reproductive toxicity by causing glycolipid metabolism dysbiosis of testis resulting in activating of the mitochondrial apoptotic pathway in spermatogenic cells. The study provides new insight into the mechanisms of male reproductive toxicity caused by BDE-209.

KeywordApoptosis Bde-209 Glycolipid Metabolism Male Reproductive Toxicity Scap/srebp-1 Pathways
DOI10.1016/j.chemosphere.2021.131512
URLView the original
Indexed BySCIE
Language英語English
WOS Research AreaEnvironmental Sciences & Ecology
WOS SubjectEnvironmental Sciences
WOS IDWOS:000704462300007
Scopus ID2-s2.0-85110406031
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Cited Times [WOS]:1   [WOS Record]     [Related Records in WOS]
Document TypeJournal article
CollectionFaculty of Health Sciences
Corresponding AuthorShi, Zhixiong; Zhou, Xianqing
Affiliation1.Department of Toxicology and Hygienic Chemistry, School of Public Health, Capital Medical University, Beijing, 100069, China
2.Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, 100069, China
3.Centre of Reproduction, Development and Aging (CRDA), Faculty of Health Sciences, University of Macau, Taipa, Macau, 999078, China
Recommended Citation
GB/T 7714
Zhang, Yue,Li, Xiangyang,Jing, Li,et al. Decabromodiphenyl ether induces male reproductive toxicity by activating mitochondrial apoptotic pathway through glycolipid metabolism dysbiosis[J]. Chemosphere,2021,285.
APA Zhang, Yue,Li, Xiangyang,Jing, Li,Zhou, Guiqing,Sang, Yujian,Gao, Leqiang,Jiang, Shuqin,Shi, Zhixiong,Ge, Wei,Sun, Zhiwei,&Zhou, Xianqing.(2021).Decabromodiphenyl ether induces male reproductive toxicity by activating mitochondrial apoptotic pathway through glycolipid metabolism dysbiosis.Chemosphere,285.
MLA Zhang, Yue,et al."Decabromodiphenyl ether induces male reproductive toxicity by activating mitochondrial apoptotic pathway through glycolipid metabolism dysbiosis".Chemosphere 285(2021).
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